Journal: Advanced Science

Article Title: Sirtuin1 Suppresses Calcium Oxalate Nephropathy via Inhibition of Renal Proximal Tubular Cell Ferroptosis Through PGC‐1α‐mediated Transcriptional Coactivation

doi: 10.1002/advs.202408945

Figure Lengend Snippet: Sirt1 inhibited CaOx‐induced ferroptosis in tubular epithelium. A) Sirt1 activation and overexpression restored the cell viability of COM‐treated HK‐2 cells evaluated by CCK‐8. B, C) Lipid peroxidation in HK‐2 cells was determined by BODIPY C11 staining and flow cytometry. D) Sirt1 activation and overexpression reduced the level of MDA in COM‐treated HK‐2 cells. Immunoblotting E) and qPCR F) revealed the expression of ferroptosis associated markers in HK‐2 cells. In vivo, mice were pretreated with SRT1720/EX527 and then induced to establish a model of CaOx nephrocalcinosis. Immunoblotting G) and qPCR H) revealed the expression of ferroptosis associated markers in HK‐2 cells. The deposition of CaOx was observed under a polarized light microscopy I) and evaluated by Pizzolato staining J). K) PAS staining was used for the scoring of tubular injury. The blue arrows highlight damaged renal tubules. L) IHC staining was performed to test the level of GPX4 and 4HNE in mouse kidney. M) The changes of mitochondrial morphology in tubular epithelium were observed by TEM. The red arrows indicate the morphologically abnormal mitochondria, characterized by mitochondrial shrinkage and disorganized cristae. N, O) The serum levels of creatinine and BUN were detected to assess kidney function. P) MDA in tissues of mice kidney was quantified. Q) The expression of KIM‐1 mRNA in tissues of mice kidney was determined by qPCR. Data were presented as mean ± SD, n = 3 for in vitro experiments and n = 6 for in vivo experiments. P value was determined by one‐way (C, D, F, H, N‐Q) or two‐way (A) ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Renal tubular epithelium‐specific Sirt1 knockout (Sirt1cKO) mice were obtained by crossing Cdh16‐Cre males (T007046, GemPharmatech Inc., China) with Sirt1 fl/fl females (T006657, GemPharmatech Inc.) on a C57BL/6J background.

Techniques: Activation Assay, Over Expression, CCK-8 Assay, Staining, Flow Cytometry, Western Blot, Expressing, In Vivo, Light Microscopy, Immunohistochemistry, In Vitro

Journal: Advanced Science

Article Title: Sirtuin1 Suppresses Calcium Oxalate Nephropathy via Inhibition of Renal Proximal Tubular Cell Ferroptosis Through PGC‐1α‐mediated Transcriptional Coactivation

doi: 10.1002/advs.202408945

Figure Lengend Snippet: Sirt1 inhibited CaOx‐induced ferroptosis in tubular epithelium dependent on GPX4.HK‐2 cells were treated with increasing concentrations of erastin, along with 5 µM SRT1720 or 1 µM Fer for 24h. A) Cell viability of HK‐2 cells was evaluated by CCK‐8. B, C) Lipid peroxidation in HK‐2 cells was determined by BODIPY C11 staining and flow cytometry. D) Level of MDA in HK‐2 cells treated with erastin, along with SRT1720 or Fer for 24 h. (E) HK‐2 cells were treated with increasing concentrations of RSL3, along with 5 µM SRT1720 or 1 µM Fer for 24 h. Cell viability of HK‐2 cells was evaluated by CCK‐8. F, G) Lipid peroxidation in HK‐2 cells was determined by BODIPY C11 staining and flow cytometry. H) Level of MDA in HK‐2 cells treated with erastin, along with SRT1720 or Fer for 24 h. I) Cell viability of Sh ctrl and GPX4 sh HK‐2 cells treated with increasing concentrations of COM and SRT1720 was evaluated by CCK‐8. J, K) Lipid peroxidation in Sh ctrl and GPX4 sh HK‐2 cells was determined by BODIPY C11 staining and flow cytometry. L) Level of MDA in Sh ctrl and GPX4 sh HK‐2 cells treated with increasing concentrations of COM and SRT1720 for 24 h. Data were presented as mean ± SD, n = 3, and P value was determined by one‐way (C, D, G, H, K, L) or two‐way (A, E, I) ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Renal tubular epithelium‐specific Sirt1 knockout (Sirt1cKO) mice were obtained by crossing Cdh16‐Cre males (T007046, GemPharmatech Inc., China) with Sirt1 fl/fl females (T006657, GemPharmatech Inc.) on a C57BL/6J background.

Techniques: CCK-8 Assay, Staining, Flow Cytometry

Journal: Advanced Science

Article Title: Sirtuin1 Suppresses Calcium Oxalate Nephropathy via Inhibition of Renal Proximal Tubular Cell Ferroptosis Through PGC‐1α‐mediated Transcriptional Coactivation

doi: 10.1002/advs.202408945

Figure Lengend Snippet: Sirt1 inhibited ferroptosis in tubular epithelium through the PGC‐1α/GPX4 pathway.A, B) Sirt1 activation and overexpression increased the protein and mRNA expression of PGC‐1α. C, D) The protein and mRNA levels of GPX4 in Sh ctrl and PGC‐1α sh HK‐2 cells treated by ZLN005. E) Cell viability of Sh ctrl and PGC‐1α sh HK‐2 cells treated with increasing concentrations of COM and SRT1720 was evaluated by CCK‐8. F, G) Lipid peroxidation in Sh ctrl and PGC‐1α sh HK‐2 cells was determined by BODIPY C11 staining and flow cytometry. Immunoblotting H) and qPCR I) revealed the expression of ferroptosis associated markers in Sh ctrl and PGC‐1α sh HK‐2 cells treated by COM and SRT1720. J) Cell viability of Sh ctrl and PGC‐1α sh HK‐2 cells treated with increasing concentrations of erastin and SRT1720 was evaluated by CCK‐8. K, L) Lipid peroxidation in Sh ctrl and PGC‐1α sh HK‐2 cells was determined by BODIPY C11 staining and flow cytometry. Immunoblotting M) and qPCR N) revealed the expression of ferroptosis associated markers in Sh ctrl and PGC‐1α sh HK‐2 cells treated by erastin and SRT1720. Data were presented as mean ± SD, n = 3, and P value was determined by one‐way (B, D, G, I, L, N) or two‐way (E, J) ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Renal tubular epithelium‐specific Sirt1 knockout (Sirt1cKO) mice were obtained by crossing Cdh16‐Cre males (T007046, GemPharmatech Inc., China) with Sirt1 fl/fl females (T006657, GemPharmatech Inc.) on a C57BL/6J background.

Techniques: Activation Assay, Over Expression, Expressing, CCK-8 Assay, Staining, Flow Cytometry, Western Blot

Journal: Advanced Science

Article Title: Sirtuin1 Suppresses Calcium Oxalate Nephropathy via Inhibition of Renal Proximal Tubular Cell Ferroptosis Through PGC‐1α‐mediated Transcriptional Coactivation

doi: 10.1002/advs.202408945

Figure Lengend Snippet: Sirt1 inhibited CaOx‐induced ferroptosis, crystal deposition and kidney injury through PGC‐1α/NRF2 signaling.A) The conditional knockout of Sirt1 in tubular epithelium in mouse kidney. B) Schematic of establishment of CaOx nephrocalcinosis model and treatment of ZLN005 and TBHQ. The deposition of CaOx was observed under a polarized light microscopy C) and evaluated by Pizzolato staining D). E) PAS staining was used for the scoring of tubular injury. The blue arrows highlight damaged renal tubules. F) IHC staining was performed to test the level of GPX4 and 4HNE in mouse kidney. G) The levels of renal ROS were detected by DHE staining. H, I) The serum levels of creatinine and BUN were detected to assess kidney function. J) MDA in tissues of mice kidney was quantified. Data were presented as mean ± SD, n = 6, and P value was determined by one‐way ANOVA (H‐J). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Renal tubular epithelium‐specific Sirt1 knockout (Sirt1cKO) mice were obtained by crossing Cdh16‐Cre males (T007046, GemPharmatech Inc., China) with Sirt1 fl/fl females (T006657, GemPharmatech Inc.) on a C57BL/6J background.

Techniques: Knock-Out, Light Microscopy, Staining, Immunohistochemistry

Journal: Scientific Reports

Article Title: Prenatal gene-environment interactions mediate the impact of advanced maternal age on mouse offspring behavior

doi: 10.1038/s41598-024-82070-x

Figure Lengend Snippet: Advanced maternal age disrupts fetal and placental development in BTBR and B6 mice. ( A ) Fetal and placental weight; **p < 0.01, ***p < 0.0001 with Mann Whitney test. ( B ) Fetal/placental weight ratio; **p < 0.01, ***p < 0.0001 with Mann Whitney test. ( C ) Correlation between fetal and placental weights were significantly different comparing AMA with YMA; **p < 0.01 with Fisher’s test. B6 YMA n = 51, B6 AMA n = 23, BTBR YMA n = 60, BTBR AMA n = 17. ( D ) Representative images depicting fetuses and placentas collected from old and young females at embryonic day 12.5; the black arrowhead indicates a resorbed conceptus.

Article Snippet: BTBR and B6 mice were purchased from Jackson Laboratory (USA) and maintained under inbreeding in the animal facility of the Institute of Genetics and Animal Biotechnology PAS in Jastrzębiec (Poland).

Techniques: MANN-WHITNEY

Journal: Scientific Reports

Article Title: Prenatal gene-environment interactions mediate the impact of advanced maternal age on mouse offspring behavior

doi: 10.1038/s41598-024-82070-x

Figure Lengend Snippet: Advanced maternal age induces changes in gene expression of fetal heads and placentas in BTBR and B6 mice. ( A ) Relative mRNA expression of several neurodevelopmental-relevant genes was decreased in AMA vs YMA fetal heads in both strains; *p < 0.05 with one-way ANOVA.

Article Snippet: BTBR and B6 mice were purchased from Jackson Laboratory (USA) and maintained under inbreeding in the animal facility of the Institute of Genetics and Animal Biotechnology PAS in Jastrzębiec (Poland).

Techniques: Expressing

Journal: Scientific Reports

Article Title: Prenatal gene-environment interactions mediate the impact of advanced maternal age on mouse offspring behavior

doi: 10.1038/s41598-024-82070-x

Figure Lengend Snippet: Delivery outcomes of young and old B6 and BTBR females, and pups’ survival to weaning.

Article Snippet: BTBR and B6 mice were purchased from Jackson Laboratory (USA) and maintained under inbreeding in the animal facility of the Institute of Genetics and Animal Biotechnology PAS in Jastrzębiec (Poland).

Techniques:

Journal: Scientific Reports

Article Title: Prenatal gene-environment interactions mediate the impact of advanced maternal age on mouse offspring behavior

doi: 10.1038/s41598-024-82070-x

Figure Lengend Snippet: The effects of maternal age on postnatal autism-like behavior are heterogeneous, depending on the genetic background and the offspring’s sex. ( A ) Number of calls on postnatal days 4 and 8. BTBR pups emit a higher number of USVs compared to B6, while no significant differences were found comparing maternal age groups. ( B ) Mean duration of USV calls. ( C ) Mean frequency of USV calls. *** denotes p < 0.0001 with the Kruskal–Wallis test. Number of pups tested: B6 YMA n = 44, B6 AMA n = 33, BTBR YMA n = 24, BTBR AMA n = 8. ( D ) Time spent in the chambers containing the social and the object stimuli by male and female offspring; *** denotes p < 0.0001 with Kruskal–Wallis test. ( E ) 3-chambered test’s social score; * denotes p < 0.05 with Kruskal–Wallis test. ( F ) Representative heatmaps of the time spent in the different locations of the 3-chambers apparatus by BTBR female offspring conceived by old and control mothers. ( G ) Number of errors made by male offspring on each testing day of the habit acquisition and the reversal learning tests. ( H ) Number of errors made by female offspring on each testing day of the habit acquisition and the reversal learning tests; ** denotes p < 0.001 and *** denotes p < 0.0001, comparing AMA vs YMA BTBR and B6 mice in each separate day, with Kruskal–Wallis test; § denotes a significant effect of the strain factor with 2-way ANOVA. ( I ) Percentage of male offspring reaching criteria of at least 80% correct trials in each testing day of the two learning phases; * denotes p < 0.05, ** denotes p < 0.01, *** denotes p < 0.001, and **** denotes p < 0.0001 comparing B6 with BTBR mice with Fisher’s exact test. ( J ) Percentage of female offspring reaching criteria of at least 80% correct trials in each testing day of the two learning phases; * denotes p < 0.05 comparing B6 with BTBR mice with Fisher’s exact test. Number of adult animals tested: males, B6 YMA n = 26, B6 AMA n = 18, BTBR YMA n = 31, BTBR AMA n = 4; females, B6 YMA n = 26, B6 AMA n = 18, BTBR YMA n = 31, BTBR AMA n = 4.

Article Snippet: BTBR and B6 mice were purchased from Jackson Laboratory (USA) and maintained under inbreeding in the animal facility of the Institute of Genetics and Animal Biotechnology PAS in Jastrzębiec (Poland).

Techniques: Control

Journal: Scientific Reports

Article Title: Prenatal gene-environment interactions mediate the impact of advanced maternal age on mouse offspring behavior

doi: 10.1038/s41598-024-82070-x

Figure Lengend Snippet: Pregnancy outcomes in young (YMA) and old (AMA) B6 and BTBR females at embryonic day 12.5.

Article Snippet: BTBR and B6 mice were purchased from Jackson Laboratory (USA) and maintained under inbreeding in the animal facility of the Institute of Genetics and Animal Biotechnology PAS in Jastrzębiec (Poland).

Techniques:

Journal: Frontiers in Pharmacology

Article Title: Antidepressant effects of ketamine: mechanisms underlying fast-acting novel antidepressants

doi: 10.3389/fphar.2013.00161

Figure Lengend Snippet: Acute effects of ketamine .

Article Snippet: Ma et al., , C57Bl/6J mice (7 wks. old 20 g) , Gutian Pharmaceutical CO. Ltd., Fuijan, China. 10 mg/kg (i.p.) , Ketamine reversed CMS-induced increases in immobility in the FST and TST 48 h post-treatment. Ketamine reversed CMS-induced reductions in sucrose intake in the SPT, 24 h, 4, 6, and 8 days post-treatment. In non-stressed animals ketamine reduced immobility in the TST and FST at 3 and 24 h post-injection , N/A.

Techniques: Injection, Expressing, Phospho-proteomics, Activity Assay, Blocking Assay, Knock-In, Produced

Journal: Frontiers in Pharmacology

Article Title: Antidepressant effects of ketamine: mechanisms underlying fast-acting novel antidepressants

doi: 10.3389/fphar.2013.00161

Figure Lengend Snippet: Protracted effects of ketamine .

Article Snippet: Ma et al., , C57Bl/6J mice (7 wks. old 20 g) , Gutian Pharmaceutical CO. Ltd., Fuijan, China. 10 mg/kg (i.p.) , Ketamine reversed CMS-induced increases in immobility in the FST and TST 48 h post-treatment. Ketamine reversed CMS-induced reductions in sucrose intake in the SPT, 24 h, 4, 6, and 8 days post-treatment. In non-stressed animals ketamine reduced immobility in the TST and FST at 3 and 24 h post-injection , N/A.

Techniques: Phospho-proteomics, Expressing, Injection, Binding Assay, Blocking Assay, Activation Assay, Activity Assay

Journal: Cardiovascular Diabetology

Article Title: Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

doi: 10.1186/s12933-015-0241-0

Figure Lengend Snippet: FGF21 deletion accelerated and aggravated diabetes-induced aortic thickening. At indicated time points after diabetes onset, histological change of aorta was evaluated by H&E staining ( a ) and aorta thickness was measured using Image Pro Plus 6.0 software ( b ). Data are presented as means ± SD, n ≥ 5 for each group. * p < 0.05 vs WT Ctrl group; # p < 0.05 vs FGF21KO Ctrl group; & p < 0.05 vs WT DM group. Bar = 50 μm. Ctrl: control; DM: diabetes mellitus; WT: wild type; FGF21KO: FGF21 knockout; m: month(s)

Article Snippet: The present study used male FGF21KO mice with C57 BL/6 J background (gifted by Dr. Steve Kliewer, University of Texas Southwestern Medical Center) [ ] and wild type (WT) C57 BL/6 J mice purchased from Jackson Laboratory (Bar Harbor, Maine).

Techniques: Staining, Software, Control, Knock-Out

Journal: Cardiovascular Diabetology

Article Title: Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

doi: 10.1186/s12933-015-0241-0

Figure Lengend Snippet: FGF21 deletion accelerated and aggravated diabetes-induced aortic fibrosis. At indicated time points after diabetes onset, aortic fibrosis was evaluated by Sirius Red staining of collagen accumulation ( a, b ) and immunohistochemical staining of CTGF expression ( c, d ). Data are presented as means ± SD, n ≥ 5 for each group. * p < 0.05 vs WT Ctrl group; # p < 0.05 vs FGF21KO Ctrl group; & p < 0.05 vs WT DM group. Bar = 50 μm. Abbreviations are the same as the Fig.

Article Snippet: The present study used male FGF21KO mice with C57 BL/6 J background (gifted by Dr. Steve Kliewer, University of Texas Southwestern Medical Center) [ ] and wild type (WT) C57 BL/6 J mice purchased from Jackson Laboratory (Bar Harbor, Maine).

Techniques: Staining, Immunohistochemical staining, Expressing

Journal: Cardiovascular Diabetology

Article Title: Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

doi: 10.1186/s12933-015-0241-0

Figure Lengend Snippet: FGF21 deficiency aggravated diabetes-induced inflammation. At indicated time points after diabetes onset, aortic inflammation was evaluated by immunohistochemical staining of TGF-β expression ( a, b ) and TNF-α ( c, d ). Plasma IL-6 was detected by ELISA ( e ). Data are presented as means ± SD, n ≥ 5 for each group. * p < 0.05 vs WT Ctrl group; # p < 0.05 vs FGF21KO Ctrl group; & p < 0.05 vs WT DM group. Bar = 50 μm. Abbreviations are the same as the Fig.

Article Snippet: The present study used male FGF21KO mice with C57 BL/6 J background (gifted by Dr. Steve Kliewer, University of Texas Southwestern Medical Center) [ ] and wild type (WT) C57 BL/6 J mice purchased from Jackson Laboratory (Bar Harbor, Maine).

Techniques: Immunohistochemical staining, Staining, Expressing, Clinical Proteomics, Enzyme-linked Immunosorbent Assay

Journal: Cardiovascular Diabetology

Article Title: Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

doi: 10.1186/s12933-015-0241-0

Figure Lengend Snippet: FGF21 deficiency accelerated diabetes-induced cell apoptosis. At indicated time points after diabetes onset, cell apoptosis was evaluated by TUNEL staining ( a, b ). Data are presented as means ± SD, n ≥ 5 for each group. * p < 0.05 vs WT Ctrl group; # p < 0.05 vs FGF21KO Ctrl group. Bar = 50 μm. Abbreviations are the same as the Fig.

Article Snippet: The present study used male FGF21KO mice with C57 BL/6 J background (gifted by Dr. Steve Kliewer, University of Texas Southwestern Medical Center) [ ] and wild type (WT) C57 BL/6 J mice purchased from Jackson Laboratory (Bar Harbor, Maine).

Techniques: TUNEL Assay, Staining

Journal: Cardiovascular Diabetology

Article Title: Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

doi: 10.1186/s12933-015-0241-0

Figure Lengend Snippet: FGF21 deficiency accelerated and aggravated diabetes-induced oxidative stress. At indicated time points after diabetes onset, oxidative stress was evaluated by immunohistochemical staining of 3-NT ( a, b ) and 4-HNE ( c, d ). Antioxidative response was also evaluated by immunohistochemical staining of transcription factor Nrf2 ( e,f ). Data are presented as means ± SD, n ≥ 5 for each group. * p < 0.05 vs WT Ctrl group; # p < 0.05 vs FGF21KO Ctrl group; & p < 0.05 vs WT DM group. Bar = 50 μm. Abbreviations are the same as the Fig.

Article Snippet: The present study used male FGF21KO mice with C57 BL/6 J background (gifted by Dr. Steve Kliewer, University of Texas Southwestern Medical Center) [ ] and wild type (WT) C57 BL/6 J mice purchased from Jackson Laboratory (Bar Harbor, Maine).

Techniques: Immunohistochemical staining, Staining

Journal: Cardiovascular Diabetology

Article Title: Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

doi: 10.1186/s12933-015-0241-0

Figure Lengend Snippet: FGF21 deficiency accelerated and aggravated the impairment of eNOS activation in diabetes. At indicated time points after diabetes onset, eNOS activation was evaluated by immunohistochemical staining of p-eNOS (Ser-1177) ( a, b ). Data are presented as means ± SD, n ≥ 5 for each group. * p < 0.05 vs WT Ctrl group; # p < 0.05 vs FGF21KO Ctrl group; & p < 0.05 vs WT DM group. Bar = 50 μm. Abbreviations are the same as the Fig.

Article Snippet: The present study used male FGF21KO mice with C57 BL/6 J background (gifted by Dr. Steve Kliewer, University of Texas Southwestern Medical Center) [ ] and wild type (WT) C57 BL/6 J mice purchased from Jackson Laboratory (Bar Harbor, Maine).

Techniques: Activation Assay, Immunohistochemical staining, Staining

Journal: Cardiovascular Diabetology

Article Title: Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

doi: 10.1186/s12933-015-0241-0

Figure Lengend Snippet: FGF21 administration reversed pathologic changes in the aorta of FGF21KO DM mice. In a type 1 diabetes model, FGF21 administration reversed aortic thickening ( a ), fibrosis ( b ) and cell apoptosis ( c ) in the aorta of FGF21KO DM mice. Data are presented as means ± SD, n ≥ 5 for each group. * p < 0.05 vs WT Ctrl group; #: P < 0.05 vs. FGF21KO Ctrl; @: P < 0.05 vs. FGF21KO DM; $: P < 0.05 vs. WT DM. Bar = 50 μm. Abbreviations are the same as the Fig. . FGF21KO DM + FGF21: FGF21KO DM mice received FGF21 administration

Article Snippet: The present study used male FGF21KO mice with C57 BL/6 J background (gifted by Dr. Steve Kliewer, University of Texas Southwestern Medical Center) [ ] and wild type (WT) C57 BL/6 J mice purchased from Jackson Laboratory (Bar Harbor, Maine).

Techniques:

Journal: Cell reports

Article Title: The histone chaperone HIR maintains chromatin states to control nitrogen assimilation and fungal virulence

doi: 10.1016/j.celrep.2021.109406

Figure Lengend Snippet:

Article Snippet: C57BL/6J mice were housed under specific pathogen-free conditions in the animal facility of the Max Perutz Labs Vienna.

Techniques: Purification, Recombinant, Saline, Protease Inhibitor, Derivative Assay, Plasmid Preparation, Software, Mass Spectrometry